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Potassium and the excitability properties of normal human motor axons in vivo.

Boërio D, Bostock H, Spescha R, Z'Graggen WJ - PLoS ONE (2014)

Bottom Line: Hyperkalemia is an important cause of membrane depolarization in renal failure.Improved modelling of potassium effects was achieved by making the potassium currents obey the constant-field theory, and by making the potassium permeabilities proportional to external potassium, as has been observed in vitro.This new model also accounted well for the changes in superexcitability and other excitability measures previously reported in renal failure.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland.

ABSTRACT
Hyperkalemia is an important cause of membrane depolarization in renal failure. A recent theoretical model of axonal excitability explains the effects of potassium on threshold electrotonus, but predicts changes in superexcitability in the opposite direction to those observed. To resolve this contradiction we assessed the relationship between serum potassium and motor axon excitability properties in 38 volunteers with normal potassium levels. Most threshold electrotonus measures were strongly correlated with potassium, and superexcitability decreased at higher potassium levels (P = 0.016), contrary to the existing model. Improved modelling of potassium effects was achieved by making the potassium currents obey the constant-field theory, and by making the potassium permeabilities proportional to external potassium, as has been observed in vitro. This new model also accounted well for the changes in superexcitability and other excitability measures previously reported in renal failure. These results demonstrate the importance of taking potassium levels into account when assessing axonal membrane dysfunction by excitability testing, and provide evidence that potassium currents are activated by external potassium in vivo.

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Potassium dependence of 2 nerve excitability measurements predicted by Models 1 (red line), 2 (green line) and 3 (blue line) compared with mean measurements for Higher K (▴), Medium K (•) and Lower K (▪) groups, and ellipse representing 1 SD limits for 9 patients with chronic renal failure (reproduced from Kiernan et al.).9Only Model 3 predicts an appropriate drop in superexcitability with increasing potassium level.
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pone-0098262-g004: Potassium dependence of 2 nerve excitability measurements predicted by Models 1 (red line), 2 (green line) and 3 (blue line) compared with mean measurements for Higher K (▴), Medium K (•) and Lower K (▪) groups, and ellipse representing 1 SD limits for 9 patients with chronic renal failure (reproduced from Kiernan et al.).9Only Model 3 predicts an appropriate drop in superexcitability with increasing potassium level.

Mentions: To further explore the potassium dependence of nerve excitability according to the 3 models, and how they predict extrapolation to hyperkalaemic levels, Figure 4 shows 2 excitability measures plotted as a function of potassium concentration, and compares the 3 models with the 3 groups of normal subjects, and also with the previously published data for patients with chronic renal failure, who had varying degrees of hyperkalemia prior to dialysis [9]. In Figure 4A it can be seen that only Model 3 predicts a marked reduction in superexcitability with increasing potassium, and when model 3 is extrapolated to abnormally high potassium levels, it predicts quite accurately the relationship previously found in patients with renal failure prior to dialysis, as indicated by the ellipse. The changes in electrotonus with potassium were too small to distinguish between the models as far as the normal subjects are concerned, but Fig 4B indicates that the changes in depolarizing electrotonus (TEd40[90–100 ms]) in the renal failure patients with hyperkalemia are also best explained by model 3.


Potassium and the excitability properties of normal human motor axons in vivo.

Boërio D, Bostock H, Spescha R, Z'Graggen WJ - PLoS ONE (2014)

Potassium dependence of 2 nerve excitability measurements predicted by Models 1 (red line), 2 (green line) and 3 (blue line) compared with mean measurements for Higher K (▴), Medium K (•) and Lower K (▪) groups, and ellipse representing 1 SD limits for 9 patients with chronic renal failure (reproduced from Kiernan et al.).9Only Model 3 predicts an appropriate drop in superexcitability with increasing potassium level.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4043986&req=5

pone-0098262-g004: Potassium dependence of 2 nerve excitability measurements predicted by Models 1 (red line), 2 (green line) and 3 (blue line) compared with mean measurements for Higher K (▴), Medium K (•) and Lower K (▪) groups, and ellipse representing 1 SD limits for 9 patients with chronic renal failure (reproduced from Kiernan et al.).9Only Model 3 predicts an appropriate drop in superexcitability with increasing potassium level.
Mentions: To further explore the potassium dependence of nerve excitability according to the 3 models, and how they predict extrapolation to hyperkalaemic levels, Figure 4 shows 2 excitability measures plotted as a function of potassium concentration, and compares the 3 models with the 3 groups of normal subjects, and also with the previously published data for patients with chronic renal failure, who had varying degrees of hyperkalemia prior to dialysis [9]. In Figure 4A it can be seen that only Model 3 predicts a marked reduction in superexcitability with increasing potassium, and when model 3 is extrapolated to abnormally high potassium levels, it predicts quite accurately the relationship previously found in patients with renal failure prior to dialysis, as indicated by the ellipse. The changes in electrotonus with potassium were too small to distinguish between the models as far as the normal subjects are concerned, but Fig 4B indicates that the changes in depolarizing electrotonus (TEd40[90–100 ms]) in the renal failure patients with hyperkalemia are also best explained by model 3.

Bottom Line: Hyperkalemia is an important cause of membrane depolarization in renal failure.Improved modelling of potassium effects was achieved by making the potassium currents obey the constant-field theory, and by making the potassium permeabilities proportional to external potassium, as has been observed in vitro.This new model also accounted well for the changes in superexcitability and other excitability measures previously reported in renal failure.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland.

ABSTRACT
Hyperkalemia is an important cause of membrane depolarization in renal failure. A recent theoretical model of axonal excitability explains the effects of potassium on threshold electrotonus, but predicts changes in superexcitability in the opposite direction to those observed. To resolve this contradiction we assessed the relationship between serum potassium and motor axon excitability properties in 38 volunteers with normal potassium levels. Most threshold electrotonus measures were strongly correlated with potassium, and superexcitability decreased at higher potassium levels (P = 0.016), contrary to the existing model. Improved modelling of potassium effects was achieved by making the potassium currents obey the constant-field theory, and by making the potassium permeabilities proportional to external potassium, as has been observed in vitro. This new model also accounted well for the changes in superexcitability and other excitability measures previously reported in renal failure. These results demonstrate the importance of taking potassium levels into account when assessing axonal membrane dysfunction by excitability testing, and provide evidence that potassium currents are activated by external potassium in vivo.

Show MeSH
Related in: MedlinePlus